ArticleJournal of the American Heart Association2013
Long-term miR-669a therapy alleviates chronic dilated cardiomyopathy in dystrophic mice.
Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 61 citations in OpenAlex.
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Review
- Identification and analysis of differentially expressed lncRNAs and their ceRNA networks in DMD/mdx primary myoblasts.Scientific reports · 2024Article
- Identification and Validation of the miR/RAS/RUNX2 Autophagy Regulatory Network in AngII-Induced Hypertensive Nephropathy in MPC5 Cells Treated with Hydrogen Sulfide Donors.Antioxidants (Basel, Switzerland) · 2024Article
- The miR-669a-5p/G3BP/HDAC6/AKAP12 Axis Regulates Primary Cilia Length.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Fulfilling the Promise of RNA Therapies for Cardiac Repair and Regeneration.Stem cells translational medicine · 2023Review
- Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis.Cells · 2023Article
- The Role of MicroRNAs in Dilated Cardiomyopathy: New Insights for an Old Entity.International journal of molecular sciences · 2022Review
- MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022Review
- Long Non Coding RNA Based Regulation of Cerebrovascular Endothelium.Frontiers in genetics · 2022Review
- Why the hype - What are microRNAs and why do they provide unique investigative, diagnostic, and therapeutic opportunities in veterinary medicine?The Canadian veterinary journal = La revue veterinaire canadienne · 2020Review
- RNA-based diagnostic and therapeutic strategies for cardiovascular disease.Nature reviews. Cardiology · 2019Review
- Core-Shell Polymer-Based Nanoparticles Deliver miR-155-5p to Endothelial Cells.Molecular therapy. Nucleic acids · 2019Article
- MicroRNAs in Cardiac Diseases.Cells · 2019Review
- Novel Therapies for Prevention and Early Treatment of Cardiomyopathies.Circulation research · 2019Review
- (Epi)genetic Modifications in Myogenic Stem Cells: From Novel Insights to Therapeutic Perspectives.Cells · 2019Review
- Epigenetics in dilated cardiomyopathy.Current opinion in cardiology · 2019Review
- Cardiac Fibroblasts and Cardiac Fibrosis: Precise Role of Exosomes.Frontiers in cell and developmental biology · 2019Review
- Review
- The Function and Therapeutic Potential of Long Non-coding RNAs in Cardiovascular Development and Disease.Molecular therapy. Nucleic acids · 2017Review
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundDilated cardiomyopathy (DCM) is a leading cause of chronic morbidity and mortality in muscular dystrophy (MD) patients. Current pharmacological treatments are not yet able to counteract chronic myocardial wastage, thus novel therapies are being intensely explored. MicroRNAs have been implicated as fine regulators of cardiomyopathic progression. Previously, miR-669a downregulation has been linked to the severe DCM progression displayed by Sgcb-null dystrophic mice. However, the impact of long-term overexpression of miR-669a on muscle structure and functionality of the dystrophic heart is yet unknown. METHODS AND
resultsHere, we demonstrate that intraventricular delivery of adeno-associated viral (AAV) vectors induces long-term (18 months) miR-669a overexpression and improves survival of Sgcb-null mice. Treated hearts display significant decrease in hypertrophic remodeling, fibrosis, and cardiomyocyte apoptosis. Moreover, miR-669a treatment increases sarcomere organization, reduces ventricular atrial natriuretic peptide (ANP) levels, and ameliorates gene/miRNA profile of DCM markers. Furthermore, long-term miR-669a overexpression significantly reduces adverse remodeling and enhances systolic fractional shortening of the left ventricle in treated dystrophic mice, without significant detrimental consequences on skeletal muscle wastage.
conclusionsOur findings provide the first evidence of long-term beneficial impact of AAV-mediated miRNA therapy in a transgenic model of severe, chronic MD-associated DCM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.